If I remember correctly, someone on twiv's podcast said that the inmune inhibition occurs months into treatment for lupus patients taking HCG. So, Could you explain in layman terms why this is not the case? Most of us have no clue about what's being discussed in the paper.

I haven't seen any evidence that (Xydroxy)chloroquine alone directly inhibits anything to do with the viral replication. The closest thing that I found is that Thymoquinone inhibits Mouse coronavirus replication and is generally protective of lungs:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933739/ https://erj.ersjournals.com/content/50/suppl_61/PA4935

Chloroquine is an antipyretic and relieves symptoms like fever from diseases like Malaria and dengue.

Chloroquine stops the inflammation from going out of control, which a good thing during an infection. But if you take it when you don't have an infection, it could stop you from detecting viruses in the first place.

The paper I cited in the previous comment mentions that Chloroquine is a TLR7 inhibitor. TLR7 is a receptor that senses of single-stranded viral RNA. https://www.sciencedirect.com/science/article/abs/pii/S01663...

There is a clinical trial going on to check for just that. The hope is that when taken as a prophylactic it prevents entry into cells and give the immune system an advantage over the pathogen, but as you say, the immunosuppressive effects are a concern. We'll see soon enough.

Repeating myself, but: there's an extent to which that trial has already been running naturally, since lots and lots of people take doses of HCQ comparable to the C19 protocol already, for rheumatoid arthritis. Lots of those people are getting C19. Are you seeing reports that arthritic patients who get C19 are faring better?

I have not seen any co-occurence statistics. As both lupus and rheumatoid arthritis are at about 1% (each), and many of them are taking HCQ, then if HCQ works[0] I would expect much fewer of them to be diagnosed with SARS-Cov-2 in the first place. This is something that the CDC _should_ be able to track, and doesn't even require any ethically questionable trials.

[0] and somehow the Lupus/RA mechanics are not influencing disease progress, which is not a trivial assumption, but does not disqualify the thought experiment entirely.

People with rheumatoid arthritis are not a good population to study. We know that certain comorbidities increase death rate. Now you have people with immune system problems taking an immunosuppressive drug. The outcome tells you nothing.

Jeremy Faust does not agree with you.

https://twitter.com/jeremyfaust/status/1246801663345618944

But it's still being given, so I'm certain there are other doctors still holding out hope.

He says "If it does work, it‘s not as good as you hope it is" and "STUDY THE DRUGS!" What he doesn't say is "lovely natural experiment" and "GREAT Stuff".

Are you seeing reports of the opposite?

Chloroquine is more toxic than Hydrochloroquine, isn't it?

IIRC the addition of the hydroxy to the drug means it's going to be more water-soluble so it would be easier to excrete in urine and flush it out of the system, which would count as "less toxic" if you squint when reading the paper

I haven't seen any detailed discussions of the differences in toxicity, but one physician made a comment to that effect.

You probably don't have to derive the relative toxicities axiomatically, since volumes appear to have been written about the lower toxicity of HCQ compared to CQ.